Tadalafil in pulmonary hypertension: May be more than seen?
Abstract
I read an interesting article about the superiority of tadalafil over tempol via its antioxidant capacity on acute hypoxia-induced pulmonary hypertension (PH) model. Rashid et al. investigated and compared the antioxidant capacity of specific phosphodiesterase type-5 (PDE5) inhibitor, tadalafil, with superoxide dismutase mimetic and an efficient free radical scavenging agent tempol in acute hypoxia-induced PH model. They demonstrated that tadalafil was superior to tempol in inhibiting hypoxia-induced rise in right ventricular systolic pressure (RVSP) without producing any fall in mean arterial pressure. Also, tadalafil was shown to partially prevent oxidative stress. In conclusion, Rashid et al. highlighted the superiority of tadalafil especially in the settings of chronic hypoxia-induced PH. Monocrotaline (MCT)-induced PH is the other widely accepted animal model in PH studies. MCT is a member of the pyrrolizidine alkaloid family of plant toxins, which induces a delayed, yet progressive vascular injury resulting in PH in rats, dogs and monkeys. It is recognized that the initial reaction to MCT-induced PH is injury to the endothelial cells that precedes media hypertrophy in small size pulmonary arteries, and leads to an increase in pulmonary artery disease. These alterations in morphology largely mimic the primary PH in humans. We have recently compared the effects of three commercially available PDE5 inhibitors: sildenafil, vardenafil and tadalafil in rat MCT-induced PH…
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Evidence Hub reads this as a editorial / letter, done in animal, not in people. Its evidence level is 5 of 5 (Very low · case / narrative / animal / in vitro / in silico). Case reports, narrative reviews, and animal, cell or computer-model studies give the weakest evidence for human health.
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